Calification of elastomer materials currently used in artificial heart fabrication and other cardiovascular devices is frequently observed after long term blood exposure. The exact cause of this problem is not clear but may be the result of lipid absorption, change in the nature of the polymer during dynamic stress, or a result of surface defects which act to trap blood components that eventually calcify. This application proposes to evaluate the cause of calcium phosphate deposition on elastomers currently used for device fabrication and also styrene-butadiene-styrene co-polymers that have been suggested as possible new materials for device fabrication. The intrinsic potential of these materials to induce calcium deposition will be evaluated. The role of dynamic stress, lipid absorption, species variation, and surface defects will be examined in a well controlled in vitro system. Inhibition of mineralization by diphosphonates will be examined. Methods of evaluation include histochemical stains, scanning electron microscopy, x-ray microanalysis, x-ray photoelectron spectroscopy, and laser microraman. The in vitro results will be compared to in vivo findings to provide a possible treatment or change in fabricaion to reduce or eliminate calcification. The success of long term implantable blood pumps is severely compromised because of premature failure of the pumping diaphragm due to calcium deposits. This work should provide information concerning the mechanism and prevention of calcification of elastomers interfacing blood. In addition, the results may provide a predictive in vitro system to evaulate calcification of new biomaterials which may interact with blood.